The effect of mixed <i>Schistosoma</i> infection on bladder morbidity and on hepatic fibrosis.

<p>OR) Odds Ratio; 95%CI) 95% Confidence Interval; Ref.) Reference category; N/A) Not Applicable; *) <i>p</i><0.05; **) <i>p</i><0.01; ***) <i>p</i><0.001.</p>a<p>The trends with age were not significant for <i>S. haematobium</i>-specific bladder morbidity, but for <i>S. mansoni</i>-specific hepatic fibrosis, they were at the level of <i>p</i><0.001 in both analyses.</p>b<p>OR for a 10-fold increase in infection intensity.</p>c<p>Mixed infections as compared to single <i>S. haematobium</i> infections.</p>d<p>Mixed infections as compared to single <i>S. mansoni</i> infections.</p

Bladder and liver co-morbidity in the two co-endemic communities studied.

<p>Number of cases.</p

<i>S. mansoni</i> egg elimination, infection intensity and bladder morbidity in subjects passing <i>S. haematobium</i> eggs in urine.

a<p>GM) Geometric Mean; 95%CI) 95% Confidence Interval.</p

Risk factors for schistosomiasis morbidity in the total study population.

<p>OR) Odds Ratio; 95%CI) 95% Confidence Interval; Ref.) Reference category; N/A) Not Applicable; *) <i>p</i><0.05; **) <i>p</i><0.01; ***) <i>p</i><0.001.</p>a<p>For <i>S. haematobium</i>-specific bladder morbidity, the trend with age was significant at the level of <i>p</i> = 0.025 in the uni- and <i>p</i> = 0.043 in the multivariable analysis. For <i>S. mansoni</i>-specific hepatic fibrosis, the trend with age was significant in the crude analysis (<i>p</i><0.001). In the adjusted analysis the ORs for hepatic fibrosis increased with age in Diokhor Tack (<i>p</i><0.001) but they did not vary with age in Ndieumeul.</p>b<p>OR for a 10-fold increase in infection intensity.</p

Age distribution of schistosomiasis morbidity in the two co-endemic communities studied.

<p>Colored stacks indicate morbidity prevalences and continuous black lines indicate mean 10log-transformed infection intensities among positive subjects with the standard error of the mean (whiskers). <b>Panel A:</b> Different forms of <i>S. haematobium</i>-specific bladder morbidity are denoted by a color gradient: light yellow stacks designate a urinary bladder score of 1, bright yellow a score of 2 and orange (3 and 4), red (5) and violet (6) indicate higher morbidity scores. The dotted red line indicates hematuria prevalence in a subsample (n = 317). <b>Panel B:</b> The severity of <i>S. mansoni</i>-specific fibrosis is denoted by a color gradient. Yellow stacks designate liver image pattern C, orange pattern D, red pattern E, and violet stacks indicate pattern F. Striped stacks designate those with borderline liver morbidity (pattern B, not classified as morbidity).</p

<i>Schistosoma mansoni</i>-associated hepatic fibrosis and <i>S. mansoni</i> infection in the two co-endemic communities studied.

a<p>GM) Geometric Mean; calculated for microscopically <i>S. mansoni</i>-positive individuals only. N/A) Not Applicable.</p

<i>Schistosoma haematobium</i>-associated bladder morbidity, hematuria and <i>S. haematobium</i> infection in the two co-endemic communities studied.

a<p>GM) Geometric Mean; calculated for microscopically <i>S. haematobium</i>-positive individuals only.</p

Cytokine Responses to <i>Schistosoma mansoni</i> and <i>Schistosoma haematobium</i> in Relation to Infection in a Co-endemic Focus in Northern Senegal

<div><p>Background</p><p>In Africa, many areas are co-endemic for the two major <i>Schistosoma</i> species, <i>S. mansoni</i> and <i>S. haematobium</i>. Epidemiological studies have suggested that host immunological factors may play an important role in co-endemic areas. As yet, little is known about differences in host immune responses and possible immunological interactions between <i>S. mansoni</i> and <i>S. haematobium</i> in humans. The aim of this study was to analyze host cytokine responses to antigens from either species in a population from a co-endemic focus, and relate these to <i>S. mansoni</i> and <i>S. haematobium</i> infection.</p><p>Methodology</p><p>Whole blood cytokine responses were investigated in a population in the north of Senegal (n = 200). Blood was stimulated for 72 h with schistosomal egg and adult worm antigens of either <i>Schistosoma</i> species. IL-10, IL-5, IFN-γ, TNF-α, and IL-2 production was determined in culture supernatants. A multivariate (i.e. multi-response) approach was used to allow a joint analysis of all cytokines in relation to <i>Schistosoma</i> infection.</p><p>Principal Findings</p><p><i>Schistosoma haematobium</i> egg and worm antigens induced higher cytokine production, suggesting that <i>S. haematobium</i> may be more immunogenic than <i>S. mansoni</i>. However, both infections were strongly associated with similar, modified Th2 cytokine profiles.</p><p>Conclusions/Significance</p><p>This study is the first to compare <i>S. mansoni</i> and <i>S. haematobium</i> cytokine responses in one population residing in a co-endemic area. These findings are in line with previous epidemiological studies that also suggested <i>S. haematobium</i> egg and worm stages to be more immunogenic than those of <i>S. mansoni</i>.</p></div

Spatial distribution of self-reported use of the different water contact sites.

<p>Black circles and crosses indicate households that were included and excluded from the analysis, respectively. Roman numerals indicate water contact sites. Blue circles indicate clusters of people that reported to frequent a given water contact site indicated by an arrow. Participants in the northeastern cluster were more likely to frequent site II (3/4 <i>versus</i> 5/273;<i>p</i> = 0.005), participants in the middle cluster to frequent site III (4/17 <i>versus</i> 2/260; <i>p</i> = 0.022), and those from the southwestern cluster to frequent site V (8/53 <i>versus</i> 1/224; <i>p</i> = 0.001) than those living outside the respective clusters.</p

Spatial distribution of <i>S. mansoni</i> and <i>S. haematobium</i> infection densities.

<p>Black circles and crosses indicate households that were included in and excluded from the analysis, respectively. Roman numerals indicate water contact sites. <b>Panel A</b> depicts the unadjusted clusters (<i>p</i> = 0.001 for both <i>S. mansoni</i> and <i>S. haematobium</i>). The geometric mean (GM) <i>S. mansoni</i> infection density was 33 epg for those living in inside the northern <i>S. mansoni</i> cluster (n = 285) compared to12 epg in the rest of the community (n = 314). The GM <i>S. haematobium</i> infection density was 4.7 ep10ml inside the southern <i>S. haematobium</i> cluster (n = 34) and 0.7 ep10ml outside (n = 565). <b>Panel B</b> depicts the gender- and age-adjusted clusters (<i>p</i> = 0.002 for <i>S. mansoni</i> (north), and <i>p</i> = 0.023 for <i>S. haematobium</i> (south).</p